What are beta-antagonists?

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its likely that the SOB (is there a light dry hacking cough as well?) is due to your use of beta blockers. did you let your physician know you have asthma? just to be ultra safe, i would call his office and let his nurse know that you are experiencing shortness of breath.

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Which beta blocker is he using?

http://www.rxlist.com/cgi/generic/advair_ad.htm

DRUG INTERACTIONS

ADVAIR DISKUS has been used concomitantly with other drugs, including short-acting beta2-agonists, methylxanthines, and intranasal corticosteroids, commonly used in patients with asthma or COPD, without adverse drug reactions. No formal drug interaction studies have been performed with ADVAIR DISKUS.

Short-Acting Beta2-Agonists: In clinical trials with patients with asthma, the mean daily need for albuterol by 166 patients using ADVAIR DISKUS was approximately 1.3 inhalations/day, and ranged from 0 to 9 inhalations/day. Five percent (5%) of patients using ADVAIR DISKUS in these trials averaged 6 or more inhalations per day over the course of the 12-week trials. No increase in frequency of cardiovascular adverse reactions was observed among patients who averaged 6 or more inhalations per day.

In a COPD clinical trial, the mean daily need for albuterol for patients using ADVAIR DISKUS 250/50 was 4.1 inhalations/day. Twenty-six percent (26%) of patients using ADVAIR DISKUS 250/50 averaged 6 or more inhalations per day over the course of the 24-week trial. No increase in frequency of cardiovascular adverse reactions was observed among patients who averaged 6 or more inhalations of albuterol per day.

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one of the active ingredients in advair is a beta2 agonist. ill get a better explanation for you. essentially, there are beta2 receptors in the heart, so there is possibility for interruption of beta2 receptor sites in the heart.

ok found something. i am bolding the pertinent informaiton, but ahve left all pharmacokinetic info for your perusal.

CLINICAL PHARMACOLOGY

Mechanism of Action: ADVAIR DISKUS: Since ADVAIR DISKUS contains both fluticasone propionate and salmeterol, the mechanisms of action described below for the individual components apply to ADVAIR DISKUS. These drugs represent 2 classes of medications (a synthetic corticosteroid and a selective, long-acting beta-adrenergic receptor agonist) that have different effects on clinical and physiological indices.

Fluticasone Propionate: Fluticasone propionate is a synthetic trifluorinated corticosteroid with potent anti-inflammatory activity. In vitro assays using human lung cytosol preparations have established fluticasone propionate as a human glucocorticoid receptor agonist with an affinity 18 times greater than dexamethasone, almost twice that of beclomethasone-17-monopropionate (BMP), the active metabolite of beclomethasone dipropionate, and over 3 times that of budesonide. Data from the McKenzie vasoconstrictor assay in man are consistent with these results.

Inflammation is an important component in the pathogenesis of asthma. Corticosteroids have been shown to inhibit multiple cell types (e.g., mast cells, eosinophils, basophils, lymphocytes, macrophages, and neutrophils) and mediator production or secretion (e.g., histamine, eicosanoids, leukotrienes, and cytokines) involved in the asthmatic response. These anti-inflammatory actions of corticosteroids contribute to their efficacy in asthma.

Inflammation is also a component in the pathogenesis of COPD. In contrast to asthma, however, the predominant inflammatory cells in COPD include neutrophils, CD8+ T-lymphocytes, and macrophages. The effects of corticosteroids in the treatment of COPD are not well defined and inhaled corticosteroids and fluticasone propionate when used apart from ADVAIR DISKUS are not indicated for the treatment of COPD.

Salmeterol Xinafoate: Salmeterol is a long-acting beta2-adrenergic agonist. In vitro studies and in vivo pharmacologic studies demonstrate that salmeterol is selective for beta2-adrenoceptors compared with isoproterenol, which has approximately equal agonist activity on beta1- and beta2-adrenoceptors. In vitro studies show salmeterol to be at least 50 times more selective for beta2-adrenoceptors than albuterol. Although beta2-adrenoceptors are the predominant adrenergic receptors in bronchial smooth muscle and beta1-adrenoceptors are the predominant receptors in the heart, there are also beta2-adrenoceptors in the human heart comprising 10% to 50% of the total beta-adrenoceptors. The precise function of these receptors has not been established, but they raise the possibility that even highly selective beta2-agonists may have cardiac effects.

The pharmacologic effects of beta2-adrenoceptor agonist drugs, including salmeterol, are at least in part attributable to stimulation of intracellular adenyl cyclase, the enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3' ,5' -adenosine monophosphate (cyclic AMP). Increased cyclic AMP levels cause relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells.

In vitro tests show that salmeterol is a potent and long-lasting inhibitor of the release of mast cell mediators, such as histamine, leukotrienes, and prostaglandin D2, from human lung. Salmeterol inhibits histamine-induced plasma protein extravasation and inhibits platelet-activating factor-induced eosinophil accumulation in the lungs of guinea pigs when administered by the inhaled route. In humans, single doses of salmeterol administered via inhalation aerosol attenuate allergen-induced bronchial hyper-responsiveness.

Understand that my understanding of this comes from being an asthmatic. I'm not a doc or nurse (though I used to be an EMT and paramedic)

The earlier meds like Alupent, Albuterol, Metaproteranol, Ventolin... (mixing brand and drug names here, sorry) tend to have the side effect of making your heart beat faster. I found that I'd get shaky too when I used my Ventolin. That's from the drug itself not being so precise in going to only the bronchial tubes, the Beta2 receptors.

Serevent works like these, but is a long-acting medication, NOT, absolutely NOT to be used in a shorteness of breath situation. But the principles of the receptors is the same.

Now that I have been using MaxAir as my emergency inhaler, I've found that I do not get those side effects, and I learned from reading the package insert that the molecule of this med more precisely targets Beta2 receptors Only.

My comment about whether you've got whatever %age of B2 receptors comes from logic only. If you've got more B2 on your heart, then even the more precise meds would have the fast heartbeat side effect as they plug into whatever B2's they find.

I'm sure it helps that these meds are inhaled, so they'll all be hitting bronchial tube receptors first no matter what.

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O/T did you ever certify in ACLS? I am studying for that now and the cardiac pharmacology is overwhelming. wheew!

o.k., so i think what just you said is that all b2 receptor sites, if b2 receptor sites are at all affected in cardiac muscle, would be affected, and not only if the heart is over 50% b2, which is what i thought you first said... which didnt make any sense.